2. Academic Validation
  3. Mechanism of neuroprotective effect of stevioside on cerebral ischemia-reperfusion injury via PPAR-γ activation

Mechanism of neuroprotective effect of stevioside on cerebral ischemia-reperfusion injury via PPAR-γ activation

  • Immunopharmacol Immunotoxicol. 2021 Dec;43(6):704-712. doi: 10.1080/08923973.2021.1966034.
Yanli Zhang 1
Affiliations

Affiliation

  • 1 Department of Neurology, Beijing Geriatric Hospital, Beijing, P.R. China.
PMID: 34448677 DOI: 10.1080/08923973.2021.1966034
Abstract

Objective: The aim of this work was to explore the possible protective effects and its mechanism of stevioside on cerebral ischemia reperfusion (CIR) induced neuron damages.

Methods: Middle cerebral artery occlusion/reperfusion (MCAO/R) rat models were constructed. The rats were treated with stevioside treatment, PPAR-γ antagonist GW9662, PPAR-γ activator pioglitazone or PI3K/Akt Inhibitor LY294002 before neurological deficits were assessed using modified Neurological Severity Scale (mNSS) scores. The infarct size, brain injury, apoptotic cells, inflammatory cytokines in neurons extracted from MCAO/R rats were determined by TTC staining, H&E staining, TUNEL staining, qRT-PCR and Western blot, respectively.

Results: Stevioside attenuates MCAO/R-induced neuronal Apoptosis and inflammation by regulating PPAR-γ expression. Besides, PPAR-γ activates PI3K/Akt signaling pathway. Moreover, PPAR-γ antagonist GW9662 or PI3K/Akt Inhibitor LY294002 abrogated the anti-apoptosis and anti-inflammatory effects of stevioside on MCAO/R rats.

Conclusion: Stevioside alleviates MCAO/R-induced neuronal Apoptosis and inflammation by upregulating PPAR-γ to activate PI3K/Akt signaling pathway.

Keywords

PI3K/AKT; PPAR-γ; Stevioside; apoptosis; middle cerebral artery occlusion/reperfusion.

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